Diseases of Mixed Etiology

Neonatal Diarrhea Complex

Etiology and Epidemiology

Diarrheal disease is documented as a very frequent cause of kid loss throughout the world (Sherman 1987). A high inci­dence of diarrheal disease is associated with intensive rearing of kids under conditions of overcrowding and poor sanita­tion.

Much has been and continues to be presumed about the causes of neonatal kid diarrhea, based on the widespread information available from calf and lamb studies. As a result, colibacillosis, caused by E. coli, is often considered to be the most common cause of diarrhea in young kids. The few epidemiologic studies actually carried out in kids, however, suggest that the nature and frequency of the vari­ous etiologic agents of diarrhea may differ considerably in the goat compared with calves and lambs, or remain unknown. In a New Zealand study, up to 72% of the diar­rhea cases in kids younger than 1 month of age remained undiagnosed regarding specific etiology (Vickers 1986).

The generally held presumption that E. coli is a major cause of diarrhea in kids is challenged by several studies (Nagy et al. 1983; Yvore et al. 1984; Polack et al. 1989; Munoz et al. 1996). In these field surveys and diagnostic laboratory investigations, cryptosporidiosis is the most commonly diagnosed cause of diarrhea in kids younger than 1 month of age, and particularly in kids younger than 15 days. The organism is rarely isolated from non-diarrheic kids. Cryptosporidiosis can occur alone or in conjunction with other presumed pathogenic bacteria, viruses, and protozoa.

The virulence attributes of gastrointestinal E. coli isolates of veterinary significance have been reviewed (DebRoy and Maddox 2001).

The ETEC are characterized by the production of heat­stable and heat-labile enterotoxins and the possession of adherence structures, known as pili or fimbriae, which allow the bacteria to colonize the intestinal lining where the enterotoxin can exert its effect on villous and crypt epi­thelial cells, producing a hypersecretory diarrhea. The ETEC are non-invasive and produce minimal lesions in the gut.

Though a major cause of diarrhea in neonatal calves, ETEC have been infrequently identified as a cause of neo­natal kid diarrhea. In a Hungarian study, the adherence pilus K99 (now also referred to as F5), which is most fre­quently associated with ETEC in calves, was rarely identi­fied in kids, though it was actively screened for. In fact, it was found in non-diarrheic kids more often than in diar- rheic kids (Nagy et al. 1987).

A number of studies from Spain have provided addi­tional information on the relationship of various E. coli types and diarrhea in kids. In one study, 210 strains of E. coli were cultured from diarrheic kids up to 3 weeks of age on 14 farms. None of the strains produced the F5 or F41 fimbrial antigens associated with ETEC in calves. Although 18 of the isolates produced F17 fimbrial antigen, none of these F17 isolates produced enterotoxin (Cid et al. 1993). A subsequent report indicated that F17-positive E. coli isolated from diarrheic kids and lambs in Spain had the phenotypic characteristic of septicemic strains and not enterotoxigenic strains (Cid et al. 1999). In another study, no E. coli possessing either the F5 or the F41 fimbriae typi­cal of ruminant ETEC were identified from fecal samples of 17 diarrheic kids up to 4 weeks of age on seven farms (Orden et al.

There is one Spanish study in which fimbriated E. coli were found frequently in diarrheic kids and lambs, but their significance was unclear because the same organisms were recovered with similar frequency from non-diarrheic kids and lambs, and none of the fimbriated isolates pro­duced enterotoxins (Munoz et al. 1996). Furthermore, the fimbriated E. coli were present in kids and lambs at approx­imately equal frequencies among the age groups - 1-5 days, 6-10 days, 11-15 days, and 16-45 days - whereas in calves ETEC are most often found in the first few days of life. Notably, the predominant pathogen isolated from diarrheic kids in this survey was Cryptosporidium parvum. It occurred mainly in kids 1-10 days of age and was not iso­lated from any non-diarrheic kids.

In contrast to the Spanish studies, there are reports from Greece suggesting that ETEC are a common cause of diar­rhea in newborn kids (Kritas 2002; Kritas et al. 2003). Isolates from kids on dairy goat farms with diarrhea in the first few days of life were confirmed as having F5 (K99) and F4 (K88) fimbriae. However, the isolates were not tested for enterotoxin and the presence of other possible pathogens, e.g., rotaviruses, was not investigated, so the etiologic role of ETEC in these outbreaks was not definitively estab­lished. The most convincing evidence offered for ETEC as the etiologic agent was that vaccination of does with a sub­unit vaccine containing K88 and K99 pilus antigens sub­stantially reduced the occurrence and severity of diarrhea in newborn kids receiving colostrum, compared to kids of unvaccinated does in a controlled study (Kritas et al.

The EPEC are also known as adhering and effacing E. coli (AEEC). They are characterized by the possession of the eae gene, which encodes intimin, an outer membrane protein that mediates intimate bacterial adhesion to host enterocytes. A second espB gene may also be involved in adhesion, but is not present in all isolates containing the eae gene. The AEEC produce characteristic attachment and effacing lesions of the gut mucosa, involving destruc­tion of the brush border of enterocytes, but are usually non-invasive.

Spanish studies on the prevalence and characteristics of AEEC in goats indicate that healthy kids and adults have a higher prevalence of AEEC than diarrheic kids, but there are differences in the characteristics of the AEEC organ­isms. AEEC from healthy kids and adults possessed both the eae and espB genes and produced verotoxin, while the isolates from diarrheic kids possessed only the eae gene and did not produce verotoxin. All kids sampled were ≤4 weeks old and the prevalence of AEEC was highest in diarrheic kids 8-14 days of age (Cid et al. 1996; de la Fuente et al. 2002). Six types of the eae gene are known, and the AEEC associated with diarrhea in kids most often pos­sessed the eaeβ type (Orden et al. 2003b). In Canada, an AEEC was identified in a 10-day-old diarrheic kid from a herd of French Alpine dairy goats in which 21 of 34 kids died over a period of three weeks with profuse diarrhea and dehydration, beginning at 1 week of age. The organism did not possess fimbrial antigens nor did it produce either enterotoxins or verotoxin, but it was eae gene positive (Drolet et al. 1994).

The EHEC are characterized by production of verotoxin, a toxin similar to the shiga toxin of Shigella dysenteriae. Some but not all EHEC are also attaching and effacing and possess the eae gene.

Though they are sometimes associated with diarrhea in ruminant hosts, the greater significance of the EHEC is in their zoonotic potential. E. coli O157:H7 is the best-known EHEC, although there are numerous other enterohemor- rhagic serotypes as well. E. coli O157:H7 is associated with diarrhea, hemorrhagic colitis, thrombocytopenic purpura, and hemolytic uremic syndrome in humans. Cattle are considered the main reservoir of the organism and there is widespread public health concern about the transmission of E. coli O157:H7 to humans through foods of bovine ori­gin. However, other livestock, including goats, can harbor verotoxigenic E. coli.

E. coli O157:H7 has been isolated from goats on commer­cial farms (Dontorou et al. 2004) and tourist farms (Pritchard et al. 2000), at agricultural fairs (Keen et al. 2006), and in petting zoos (DebRoy and Roberts 2006). It has been associated with hemorrhagic colitis and hemo­lytic uremic syndrome in humans through foods of caprine origin, including unpasteurized milk (Bielaszewska et al. 1997; McIntyre et al. 2002) and fresh unpasteurized goat cheese (Espie et al. 2006), and possibly by direct con­tact with goats or goat feces (Pritchard et al. 2000; Heuvelink et al. 2002).

EHEC serovars other than O157 are found more com­monly in goats. For instance, a fatal case of diarrhea in a 2-month-old goat was confirmed as being due to a vero- toxic E. coli serotype O103:H2 (Duhamel et al. 1992). In a German study, 70 verotoxin-producing strains were iso­lated from 93 healthy goats from six farms. None was O157 and only one possessed the eae gene (Zschock et al. 2000). In another German study, 37 of 66 healthy goats yielded verotoxin-producing strains and none was 0157. The pre­dominant serotype (70%) was O5:H^- with single isolates of O82:H8, O87:H21, O5:H10, and O74:H^-, as well as nine untypeable strains also recorded (Beutin et al.

Other pathogenic E. coli that can infect ruminant neo­nates are primarily associated with septicemia rather than enteritis. Some of these may be necrotoxigenic strains of E. coli (NTEC) that produce CNF. Others may belong to known invasive serotypes. In colisepticemia, invasive strains of E. coli gain entrance to the bloodstream and pro­duce clinical disease through the effects of bacteremia and endotoxemia. Diarrhea may be part of the clinical syn­drome, but is not the primary problem. Colisepticemia occurs most commonly in neonates that have not received adequate passive immunity through consumption of the dam's colostrum. The condition is discussed further in Chapter 7 in the section on failure of transfer of passive immunity.

In a New Zealand study, C. perfringens types C and D were rarely identified as causes of diarrhea in kids. Enterotoxemia is considered to more commonly assume the neurologic or sudden death forms than the enteric form in New Zealand (Vickers 1986).

Rotaviruses have been identified from diarrheic kids for over 30 years, and serologic surveys indicate a high preva­lence of infection in goats in some countries - for example 60% in Japan (Takahashi et al. 1979), 41% in Turkey (Gumusova et al. 2007), and 25.7% in Italy (Iovane et al. 1988). It is reported to be the most common enteric virus of goats in New Zealand, and is believed to cause pro­fuse diarrhea either alone or in combination with E. coli and/or cryptosporidia (Thompson 2001).

However, the epidemiology of rotavirus as a cause of neonatal diarrhea in kids still requires further clarification. In an early report from the United Kingdom, rotavirus par­ticles were identified from the diarrheic feces of several 4-month-old goatlings (Scott et al. 1978). If the virus was indeed responsible for the diarrhea, this would be in marked contrast to rotavirus infection in calves and lambs, where clinical diarrhea is unusual in individuals older than 3 weeks of age. In France, rotaviruses were identified read­ily from non-diarrheic kids with almost equal frequency as from diarrheic kids, raising questions about their patho­genicity in goats (Yvore et al. 1984).

Rotaviruses are now known to belong to eight different serogroups, A through H, based on the cross-reactivity of antibodies to the major inner capsid protein, VP6. Group A rotaviruses are most commonly associated with diarrhea in farm animals. Rotavirus A was identified as the cause of diarrhea in 12-16-week-old Saanen kids in South Africa (Costa Mendes et al. 1994). The presence of rotavirus A was also confirmed in Canada in 1-2-week-old goat kids with diarrhea in conjunction with cryptosporidial infection. Rotavirus A was considered to be contributory to the diar­rhea, because villous atrophy was more pronounced histo­logically in kids with dual infection than in kids with cryptosporidiosis alone (Sanford et al. 1991). In contrast, no association between group A rotavirus and diarrhea in kids could be made in a Spanish goat herd where rotavirus was identified in the feces of five times as many normal kids as diarrheic kids (Munoz et al. 1994).

Group B rotavirus was identified in Spain as the sole cause of severe diarrhea, dehydration, and prostration in kids 2-3 days of age and affecting 22.6% of kids on the farm (Munoz et al. 1995). In a broader survey of diarrheic and healthy kids on 16 goat farms in Spain, group A, B, and C rotaviruses were identified. Group A rotaviruses were iden­tified in healthy kids more often than in diarrheic kids, while group C rotavirus was identified in healthy kids only. An association between infection and diarrhea was estab­lished only for the group B rotaviruses (Munoz et al. 1996).

Coronavirus is a major cause of diarrhea in calves, but information on coronavirus infection in goats is limited. A seroprevalence study in five provinces in Turkey found 41% of goats sampled positive for bovine coronavirus (Gumusova et al. 2007). There are no published reports of diarrhea outbreaks in kids confirmed as due solely to coro­navirus. Some disease investigations in diarrheic kids have actively screened for the presence of coronavirus as an etio­logic agent. Either coronavirus was not found at all (Munoz et al. 1996) or it was present at a low prevalence, almost always in mixed infections with other likely causative agents, notably cryptosporidia or ETEC (Nagy et al. 1983; Ozmen et al. 2006). These findings suggest that coronavi­rus is a possible but unlikely contributor to the neonatal disease complex in kids.

Adenoviruses are not commonly associated with diar­rhea in kids. Adenoviruses were identified in diarrheic goats in Hungary (Nagy et al. 1983). They also have been isolated from the intestine of two goats in Nigeria that died of PPR (Gibbs et al. 1977), as well as from goats in Senegal during PPR outbreaks (Nguyen et al. 1988). Because PPR is a major known cause of diarrhea, it is difficult to ascribe significance to the adenovirus. Also, a new serotype of ade­novirus was isolated from a 3-week-old kid with diarrhea and respiratory disease in California (Lehmkuhl et al. 2001). It was one of about 50 kids from a 900-doe herd showing similar signs.

Yersinia spp., Giardia, and Campylobacter jejuni were confirmed as causes of diarrhea in New Zealand (Vickers 1986). C. jejuni has also been isolated from diar­rheic feces of kids in Nigeria (Adetosoye and Adeniran 1987) and Canada (Prescott and Bruin-Mosch 1981). Again, the role of this organism remains equivocal because, in the Canadian study, C. jejuni was also isolated from the feces of normal goats.

Infection with the flagellated protozoa Giardia duodena- lis (syn. Giardia intestinalis, Giardia lamblia) has been reported from most continents and has been identified in all the common agricultural animals, but is not always associated with disease (Constable et al. 2017). Cysts of G. duodenalis are frequently found in the feces of healthy animals and, when present in diarrheic animals, they are often present with other potential etiologic agents, so attri­bution of pathogenicity remains equivocal. This reflects the situation in goats as well. Several prevalence studies have been reported. In Spain, 19.8% of adult goats were infected in one survey and 33% in another (Castro-Hermida et al. 2007a,b). In pregnant does, shedding of cysts in feces increased 7-10 times in the three weeks around kidding time (Castro-Hermida et al. 2005a). In France, goats on 100% of 20 farms shed G. duodenalis cysts and on-farm prevalence ranged from 10 to 80%, with an overall rate of 38%. Prevalence was highest in kids 6-8 months of age (Castro-Hermida et al. 2005b). In Romania, 16-18% of adult goats were infected in both pasture and housed envi­ronments, while 10-50% of kids were infected, with pastured kids having higher prevalence than intensively reared kids (Suteu et al. 1987).

Experimental infection of goats has been reported, indi­cating that G. duodenalis is capable of producing enteric disease by itself, though only three of eight challenged kids developed loose stool, depression, and decreased appetite (Koudela and Vitovec 1998). In reports of naturally occur­ring infection associated with diarrheal disease, G. duode- nalis is usually identified in association with other potential etiologic agents such as C. parvum (Sutherland 1982; Sutherland and Clarkson 1984; Ozmen et al. 2006) or coc- cidia and trichostrongyles (Suteu et al. 1987). It is reason­able to consider G. duodenalis as a pathogen when found in kids with diarrhea, but other potential causes should be investigated, and the presence of the organism in adults does not necessarily mean that the organism will cause problems in kids. When Giardia is present in herds, how­ever, managers and veterinarians must be cognizant of the fact that the organism has zoonotic potential as a cause of diarrhea in humans.

Caprine herpesvirus infection has been associated with diarrhea in kids. Herpesvirus infection was first recognized in California in 1972 in association with a severe general­ized infection of 1-2-week-old French Alpine kids, causing increased morbidity and mortality rates (Saito et al. 1974). A similar outbreak of disease characterized by fever and ulcerative enteritis with high mortality in kids was recorded in dairy goats in Switzerland in 1978 (Mettler et al. 1979). Affected kids show signs of weakness, dyspnea, cyanosis, abdominal pain, diarrhea, nasal discharge, and oral ero­sions. Not all signs are present in all individual kids. The disease has a fatal course of one to four days. Necrosis and ulceration of the digestive tract, especially the cecum and colon, are prominent necropsy findings. More detailed information on other manifestations of herpesvirus infec­tion in goats is found in Chapter 12 and elsewhere in this text.

These limited studies suggest that the conventional wis­dom about the etiologic basis of infectious diarrhea in young goat kids, largely extrapolated from experience with calves and lambs, bears further examination. Enterotoxigenic E. coli may be involved less often than is generally assumed. Veterinarians working up diarrhea out­breaks in kids should specifically seek to establish the pres­ence and characteristics of ETEC, but should also be looking to identify other likely bacterial, viral, protozoal, and/or non-infectious causes of diarrhea in young goats. C. parvum appears to be a more significant cause of diar­rhea in the first week of age, with rotaviruses also playing a potentially important role. Multiple agents may be present and their contributory importance and possible interac­tions need to be further clarified. More local diagnostic surveys should be undertaken wherever goats are raised, because appropriate recommendations for treatment and control may depend on more accurate knowledge of causa­tive agents.

Infectious agents may not always be involved in diarrhea of young kids. Many cases may be nutritionally based and difficult to diagnose at post mortem without adequate feed­ing and management history, which may be difficult to obtain after the fact.

Nutritional causes of diarrhea in young kids are often associated with husbandry and feeding practices. Problems identified include overfeeding of milk, using poor-quality milk replacers, suddenly changing the feeding routine, and switching to cow milk replacers. Incorrect mixing and dis­pensing of milk replacer by a malfunctioning automatic feeder have been reported as a cause of kid diarrhea (Lane 1987). These situations may produce non-infectious diarrhea, or predispose to the proliferation of pathogenic bacteria in the abomasum, rumen, or intestine.

When kids reach 1 month of age, the common causes of diarrhea are better established. Coccidiosis is likely the most common and helminthiasis the second most common prevailing identifiable cause of diarrhea in weaned, grow­ing kids worldwide. Other well-known causes of diarrhea in older kids also include enterotoxemia caused by C. per­fringens type D, salmonellosis, yersiniosis, PPR, and indi­gestion associated with the transition to solid feeds. These are either more sporadic or more geographically restricted than coccidiosis and helminthiasis.

Pathogenesis

Diarrhea, as a pathophysiologic process, results in dehy­dration, acidosis, and electrolyte depletion, and in neo­nates is also associated with hypoglycemia. These physiologic derangements, when unchecked, are often fatal. Certain agents such as Salmonella spp. and C. perfrin- gens, though primarily enteric pathogens, can cause marked, concurrent systemic effects in addition to diarrhea as a result of bacteremia and toxemia, respectively. Certain agents may produce clinical effects in multiple organ sys­tems, as exemplified by the pneumoenteritis syndrome seen in PPR.

Clinical Findings

In the case of diseases limited to the gastrointestinal tract such as cryptosporidiosis, enteropathogenic colibacillosis, and the enteric viruses, diarrhea is the predominant clini­cal sign. The character of diarrheic feces in kids can vary considerably, from pasty white to loose yellowish green, to watery brown, and it is inadvisable to ascribe too much diagnostic significance to the color or consistency of feces in a given case, especially because mixed etiologies are possible. Streaking of feces with blood may also be seen with a variety of causative agents. Regardless of cause, there may be some degree of abdominal discomfort, possi­ble abdominal distension, and probable loss of appetite in association with diarrhea. Giardiasis has been reported to assume a chronic form in kids and lambs lasting several weeks with gassy, watery brown feces (Ozmen et al. 2006).

If diarrhea is prolonged or severe, then dehydration ensues. Dehydrated animals become depressed, the mouth is dry, and they gradually lose the sucking reflex. Affected animals grow progressively weaker until they are unable to stand. Loss of body fluid produces hypovolemia and poor peripheral circulation. Extremities feel cold, the skin pinch reaction becomes slowed, the eyeballs become sunken, and the body temperature may become subnormal. Electrolyte and acid-base imbalances resulting from diarrhea may lead to neurologic disturbances, including hyperesthesia and opisthotonus or terminal convulsions. Loss of bicarbo­nate in the diarrheic feces and a buildup of L-lactate due to the poor peripheral perfusion associated with dehydration combine to produce a severe metabolic acidosis in diar- rheic, dehydrated kids, which is life threatening.

Clinical Pathology and Necropsy

Measurement of PCV, total plasma protein, serum sodium, potassium, bicarbonate, blood glucose, and blood gases is useful in determining the severity of electrolyte deficits, acidosis, and hypoglycemia in neonatal diarrhea cases. In the field, however, useful estimates of these deficits can also be gauged based on the severity of clinical dehydra­tion. In general, diarrheic kids have a hyperkalemic, meta­bolic acidosis with a high serum anion gap.

Submission of diarrheic feces to a diagnostic laboratory for etiologic evaluation is encouraged. At the very mini­mum, samples from kids younger than 3 weeks of age should be evaluated for cryptosporidia, enterotoxigenic and enteropathogenic E. coli, Salmonella, rotavirus, and coronavirus. In kids older than 3 weeks of age, additional evaluations should include coccidiosis, giardiasis, entero­toxemia, and yersiniosis. Samples should be collected within 12-24 hours of the onset of diarrhea, because the viruses may be rapidly cleared from the gut. A volume of 5-10 cc of fresh, diarrheic feces should be submitted under refrigeration. If such volumes are unavailable and rectal swabs are used, they should be shipped to the lab in a suit­able bacterial transport medium. Also, fresh fecal smears prepared on glass slides can be valuable in the diagnosis of cryptosporidiosis and enteric viruses by acid-fast staining and fluorescent antibody testing, respectively. Survival of cryptosporidial oocysts in fresh feces is poor. While viruses can be identified in fresh feces by electron microscopy, such equipment is not always available. Many virulence factors associated with the various types of E. coli can be identified using molecular techniques such as gene probes and multiplex PCR to help characterize isolates from neo­natal diarrhea cases. These techniques have been reviewed (DebRoy and Maddox 2001).

At necropsy, a loop of bowel can be ligated and removed, and submitted to the lab unopened under refrigeration. Formalinized tissues from major organs and various por­tions of the gastrointestinal tract should also be submitted for histopathologic evaluation. Gross lesions may be found at necropsy in the case of coccidiosis, salmonellosis, yers- iniosis, enterotoxemia, and some forms of gastrointestinal nematodiasis, and these lesions are discussed under each of these disease headings elsewhere in the chapter. The remainder of the causes of diarrhea in young kids may pro­duce few or no gross abnormalities beyond some gaseous distension of the bowel and slight hyperemia. Histologic evaluation can be helpful in some of these cases and immu­nohistochemistry is now also available for identification of some enteric pathogens, for example Cryptosporidium and Giardia.

Diagnosis

Definitive diagnosis of the causes of diarrhea in young kids may require exhaustive and costly bacteriologic, virologic, and parasitologic testing in the diagnostic laboratory. For some etiologic agents, rapid field diagnostic tests have become available. Based on later flow immunochromato­graphic techniques, monoclonal antibody-impregnated test strips will bind with specific antigens in the feces and form a positive, colored test line after a short incubation. Such tests are available for several causative agents of neo­natal diarrhea in goats, including C. parvum, G. duodena- lis, C. perfringens, and rotavirus. Antigens of multiple agents may be present in the same sample, so ascribing causality to a single agent is problematic (Ozcelik and Balikci 2018). A list of likely causes of diarrhea in young kids based on age is given in Table 10.3 to serve as a general diagnostic guideline.

Treatment

Many of the common causes of diarrhea are self-limiting, and the major goals of therapy are to keep the kid physio­logically stable while the diarrhea runs its course. Implementation of this strategy includes moving the kid to a warm, dry place to maintain proper body temperature, and providing appropriate fluid therapy to counter dehydra­tion, electrolyte depletion, hypoglycemia, and acidosis. Oral or parenteral therapy can be used depending on the severity of disease. Oral fluids can be used in kids up to 7% dehydra­tion, but they should receive intravenous fluids with bicar­bonate supplementation if dehydration level exceeds 8%. Many commercial preparations are manufactured for oral rehydration therapy in diarrheic animals and are increas­ingly available worldwide. Effective oral rehydration prepa­rations should contain sodium chloride, potassium chloride, sodium bicarbonate, glucose, and glycine. The basic intra­venous fluids should contain equal volumes of isotonic saline, isotonic sodium bicarbonate, and isotonic dextrose, but additional amounts of isotonic bicarbonate (1.3%) likely need to be given to correct the bicarbonate deficit associated with severe diarrhea. Additional details on the manage­ment of parenteral therapy in diarrheic neonates are avail­able elsewhere (Constable et al. 2017).

The feeding of milk or milk replacer products should be approached cautiously during the acute phase of diarrhea. Because there likely will be some derangement of digestive function, lactose in milk-based feeds may remain undi­gested in the gut and promote a hyperosmotic diarrhea on top of the existing enteritis. Alternating oral electrolyte solutions with small feedings of milk is a reasonable approach. The use of commercial, lactose-free milk prod­ucts or the addition of commercially available lactase enzyme (e.g., Lactaid) to goat milk before feeding to kids may also be useful. Kids should be brought back on milk gradually as diarrhea improves. In diarrhea that lasts for more than several days, it is necessary to feed milk prod­ucts to avoid starvation. The strategy then becomes to decrease the volume fed per feeding and to increase the number of feedings. In this manner, the residual digestive capacity of the gut may not be overwhelmed.

A variety of oral anti-diarrheal medications and intesti­nal protectants such as bismuth subsalicylate or kaolin/ pectin have been used in kids. They may be helpful, but no efficacy trials have ever been reported in goats. Similarly, oral yogurt or lyophilized Lactobacillus cultures are given empirically to restore a more normal gut flora.

Whenever possible, antibiotic therapy for diarrhea should be based on culture and sensitivity tests. When bac­terial causes of diarrhea are strongly suspected and sensi­tivity testing is not possible, then broad-spectrum oral or parenteral antibiotic therapy such as trimethoprim/sulfa may be indicated. More details on specific antibiotic choices are given in the separate discussions of each bacte­rial disease elsewhere in this chapter. Antibiotics are some­times used indiscriminately by goat owners in lieu of diagnostic veterinary services, and client education is an important part of managing diarrhea outbreaks, particu­larly with regard to growing concerns about the danger of antimicrobial resistance.

Control

Regardless of the etiologic cause, one of the most effective means of controlling the spread of diarrhea in kid populations in the face of an outbreak is to immediately and strictly isolate affected kids at the first sign of diarrhea. When possible, other exposed kids should be moved to a clean pen, or at least temporarily removed from diarrhea- contaminated pens to permit disinfection. In the case of viral enteritides and cryptosporidiosis, where effective therapeutic agents may not be available, the use of isola­tion and sanitation as control measures becomes critical.

Diarrhea in kids, as with other species, is likely to be more common in intensive rearing operations. In these situations, kids should be born in clean, draft-free quarters and not allowed to become chilled. They should receive adequate colostrum as early in life as possible, at least before 6 hours of age. Colostrum banks may be helpful in ensuring an adequate supply of colostrum. Outbreaks of diarrhea often occur at the end of the kidding season, indi­cating that there is a progressive buildup of pathogens over time and that better sanitation is needed in kidding areas, kid housing areas, and feeding equipment.

Vaccination of the doe in the four to six weeks before kid­ding may improve the concentration and specificity of pro­tective antibodies available in the colostrum. Vaccination of the dam with C. perfringens types C and D is already justi­fied. Bovine K99+ E. coli vaccines have been demonstrated to produce increased K99-specific antibody in doe serum and colostrum (Contrepois and Guillimin 1984). A subunit vaccine for pigs containing K88 and K99 pilus antigens reduced diarrhea in a herd when does were vaccinated and kids consumed their colostrum (Kritas et al. 2003). The eco­nomic justification for using such vaccines depends on con­firmation that ETEC are involved in diarrheal outbreaks on the farm or in the veterinarian’s practice area. It is also unknown if bovine rotavirus and coronavirus vaccines are effective in the control of diarrhea in young goats. In endemic areas, vaccination of goats for PPR is justified.

Kids should be housed separately or in small groups of approximately equal age. Bedding should be clean and dry. Regardless of feeding system, all utensils and equipment should be cleaned and disinfected between feedings. In ad libitum feeding systems, a small amount of formalin has been added to milk to inhibit bacterial overgrowth in the milk and the kids’ gastrointestinal tract. Kids should be offered access to hay soon after birth and a grain ration offered by week two to initiate good rumen development and a normal flora, and to avoid subsequent weaning shock. When possible, kid pens should be organized so that feed can be fed in trays or buckets outside the pen to avoid fecal contamination of feedstuffs.